A 58-year-old woman with hypertension was referred to our cardiology lipid clinic, as she had new onset of hypertriglyceridemia. She has a past medical history of asthma and GERD but there is no known history of diabetes mellitus, dyslipidemia, or a familial history of known lipid disorders. She is very active, exercises regularly and drinks 1-2 glasses of wine with meals several times each week.
Patient's medications include Esomeprazole 40mg, Montelukast 10mg once daily, Lisinopril 20mg daily, and Metoprolol succinate 50mg daily for treatment of hypertension.
On exam, her blood pressure is 142/90, pulse 74, weight 128 pounds, height 5 foot 3 inches and BMI 22.7.
Physical exam was unremarkable and without stigmata of hyperlipidemia.
Her fasting glucose is 102, A1c 5.3, total cholesterol 257, triglycerides 734, HDL 45 and calculated LDL 65. A repeated lipid panel that was known to be conducted in the fasting state confirmed very high triglycerides.
A triglyceride level obtained several years earlier was 169.
In addition to recommending alcohol cessation, what is the most appropriate next step in the management of this patient?
Show Answer
The correct answer is: C. Specific adjustments to existing medical regimen
The patient has hypertriglyceridemia of recent onset, indicating a secondary cause for the marked elevation in TG levels. The most likely etiology is medication related and of the medications listed, β blockers are the most likely culprit.
β blockers lead to unopposed α-receptor activation, catecholamine release and inhibition of lipoprotein lipase, a primary mediator of TG hydrolysis. Consequently, TG levels can rise dramatically as demonstrated in this patient. Following discontinuation of metoprolol, her triglycerides were reduced by two-thirds within two months, thereby edging closer to levels seen several years earlier.
Choice A is incorrect. While aerobic activity effectively reduces TG (~20-30% on average) this patient is already active. Therefore, additional exercise is less likely to be as impactful in reducing TG levels.
Choice B is incorrect. A high carbohydrate diet raises TG, especially when carbs intake exceeds 60-65% of energy intake, due to enhanced hepatic secretion of VLDL.
Choice D would be correct as the first step in therapy if the patient had a prior history of pancreatitis. While TG levels above 500 are associated with increased risk of pancreatitis, the overall likelihood is low (10-20%). Therefore it is reasonable to first determine whether reversible etiologies are present. Otherwise the decision to add new medications would only serve to treat a secondary condition caused by another medication. In fact, careful history taking in this case revealed that the patient was placed on metoprolol shortly after being diagnosed with hypertension about two years earlier. Had a lipid level been drawn after initiation of this medication, the diagnosis of high TG would likely have been made at that time.
Choice E might be considered after reversible causes had been ruled out or had pancreatitis been more strongly suspected. A GI workup would not be the best initial choice in this case.
References
Day JL, Metcalfe J, Simpson CN, Adrenergic mechanisms in control of plasma lipid concentrations. Br Med J 1982; 284:1145-1148.
Miller M, Stone NJ, Ballantyne C, Bittner V, Criqui MH, Ginsberg HN, Goldberg AC, Howard WJ, Jacobson MS, Kris-Etherton PM, Lennie TA, Levi M, Mazzone T, Pennathur S; American Heart Association Clinical Lipidology, Thrombosis, and Prevention Committee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Nursing; Council on the Kidney in Cardiovascular Disease. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation 2011;123:2292-2333. [See table 5].
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